Abstract
Oxidative stress is an important factor of myocardial hypoxia/reoxygenation (H/R) injury. Our research focuses on how to reduce the cardiac toxicity caused by oxidative stress through natural plant extracts. Vanillic acid (VA) is a phenolic compound found in edible plants and rich in the roots of Angelica sinensis. Experimental studies have provided evidence for this compound's effectiveness in cardiovascular diseases; however, its mechanism is still unclear. In this study, molecular mechanisms related to the protective effects of VA were investigated in H9c2 cells in the context of H/R injury. The results showed that pretreatment with VA significantly increased cell viability and decreased the percentage of apoptotic cells, as well as lactate dehydrogenase and creatine phosphokinase activity, in the supernatant, accompanied by reduced levels of reactive oxygen species and reduced caspase-3 activity. VA pretreatment also restored mitochondrial membrane potentials. Moreover, preincubation with VA significantly attenuated mitochondrial permeability transition pore activity. VA administration upregulated adenosine monophosphate-activated protein kinase α2 (AMPKα2) protein expression, and interestingly, pretreatment with AMPKα2-siRNA lentivirus effectively attenuated the cardioprotective effects of VA in response to H/R injury.
Highlights
Myocardial hypoxia/reoxygenation (H/R) injury leads to significant morbidity and mortality [1], and oxidative stress is one of the most important factors causing cardiac toxicity
To measure the effects of Vanillic acid (VA) on H9c2 cells undergoing hypoxia/reoxygenation (H/R), MTS assay was performed on H9c2 cells that were pretreated with different concentrations of VA 24 h prior to H/R
We demonstrated that VA significantly increased H9c2 cell viability
Summary
Myocardial hypoxia/reoxygenation (H/R) injury leads to significant morbidity and mortality [1], and oxidative stress is one of the most important factors causing cardiac toxicity. Our research focuses on the use of natural plant extracts to protect the heart against oxidative stress, thereby reducing cardiac toxicity caused by I/R injury. Adenosine monophosphate-activated protein kinase (AMPK) is a stress responsive kinase that modulates a number of physiologically and metabolically significant pathways, including apoptosis, energy dynamic balance, and cellular metabolism [12]. AMPK ameliorates cellular antioxidant enzyme systems, such as manganese superoxide dismutase (Mn-SOD) and catalase, reducing oxidant-induced injury [13]. We hypothesized that VA exerts a protective effect against hypoxia/reoxygenation (H/R) injury, which might be related to the AMPK signalling pathway. Oxidative Medicine and Cellular Longevity cells from hypoxia/reoxygenation (H/R) injury and (2) explore the underlying protective mechanisms of VA on hypoxia/reoxygenation (H/R) injury in H9c2 cells
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
